| Literature DB >> 26808241 |
Quaiser Saquib1, Maqsood A Siddiqui2, Javed Ahmed2, Abdullah Al-Salim2, Sabiha M Ansari3, Mohammad Faisal3, Abdulaziz A Al-Khedhairy4, Javed Musarrat5, Hend A AlWathnani3, Abdulrahman A Alatar3, Saud A Al-Arifi4.
Abstract
We have evaluated the in vitro low dose hepatotoxic effects of two flame-retardants (BDE-47 and BDE-32) in HepG2 cells. Both congeners declined the viability of cells in MTT and NRU cell viability assays. Higher level of intracellular reactive oxygen species (ROS) and dysfunction of mitochondrial membrane potential (ΔΨm) were observed in the treated cells. Comet assay data confirmed the DNA damaging potential of both congeners. BDE-47 exposure results in the appearance of subG1 apoptotic peak (30.1%) at 100 nM, while BDE-32 arrested the cells in G2/M phase. Among the set of 84 genes, BDE-47 induces downregulation of majority of mRNA transcripts, whilst BDE-32 showed differential expression of transcripts in HepG2. The ultrastructural analysis revealed mitochondrial swelling and degeneration of cristae in BDE-47 and BDE-32 treated cells. Overall our data demonstrated the hepatotoxic potential of both congeners via alteration of vital cellular pathways.Entities:
Keywords: BDE-32; BDE-47; Cell death; Flame-retardants; Oxidative stress
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Year: 2016 PMID： 26808241 DOI： 10.1016/j.jhazmat.2016.01.025
Source DB: PubMed Journal: J Hazard Mater ISSN： 0304-3894 Impact factor: 10.588